Vein graft intimal hyperplasia involves an abnormal migration and proliferation of vascular smooth muscle (VSM) cells. The end result is a thickening of the intima, reduced luminal area and potential for thrombotic occlusion. This process limits the effectiveness of reversed saphenous vein graft bypass as a treatment of coronary artery stenosis. VSM proliferation may be dependent on signal transduction, which involves Gbeta gamma subunits. The beta-adrenergic receptor kinase carboxyl terminus (betaARKCt) is a peptide inhibitor of Gbeta gamma signaling. The central hypothesis is that gene transfer of the betaARKct aortocoronary vein grafts will reduce intimal hyperplasia. Develop and characterize a swine model of intimal hyperplasia in aortocoronary vein grafts. Achieve transgene expression in vein graft smooth muscle cells employing recombinant replication deficient, adenoviral vectors, and study the impact of betaARKct transgene expression on intimal hyperplasia. Study molecular mechanisms of the betaARKct antiproliferative effect on vascular smooth muscle cells in vitro.